Angiostrongylus vasorum, a small metastrongylid nematode, inhabits the right heart and pulmonary arteries of dogs and related carnivores. Clinical abnormalities associated with canine angiostrongylosis involve the cardiopulmonary system and the hemostatic mechanism. Congestive heart failure, consolidation and fibrosis of the lungs, eosinophilia, edema of dependent portions of the body, shifting lameness, prolonged clotting times, and death have been reported. Experimental infections produce predictable pulmonary thromboemboli and disturbances in hemostasis. Whole worm homogenates of adult helminths specifically inhibit Factor XIIa (activated Hageman factor). The studies proposed herein will delineate pathophysiological changes associated with experimentally induced canine angiostrongylosis by placing special emphasis on detecting and evaluating changes in the hemostatic mechanism and the pulmonary vasculature. This will be accomplished by using a battery of hematologic, physiologic, and radiologic examinations throughout the course of infection and correlating these findings with post-mortem findings. Additional insight into the basic mechanism involved with formation of thromboemboli will be obtained via study of ultrastructual changes in the vasculature and by establishing sterile infections through transplantation of male worms. In vivo activity of the Factor XIIa inhibitor will be sought by injecting homogenates of adult worms.